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    SOX7 expression is critically required in FLK1-expressing cells for vasculogenesis and angiogenesis during mouse embryonic development.

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    Authors
    Lilly, Andrew J
    Mazan, Andrzej
    Scott, D
    Lacaud, Georges
    Kouskoff, Valerie
    Affiliation
    Cancer Research UK Manchester Institute, The University of Manchester, Wilmslow road, M20 4BX
    Issue Date
    2017-08
    
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    Abstract
    The transcriptional program that regulates the differentiation of endothelial precursor cells into a highly organized vascular network is still poorly understood. Here we explore the role of SOX7 during this process, performing a detailed analysis of the vascular defects resulting from either a complete deficiency in Sox7 expression or from the conditional deletion of Sox7 in FLK1-expressing cells. We analysed the consequence of Sox7 deficiency from E7.5 onward to determine from which stage of development the effect of Sox7 deficiency can be observed. We show that while Sox7 is expressed at the onset of endothelial specification from mesoderm, Sox7 deficiency does not impact the emergence of the first endothelial progenitors. However, by E8.5, clear signs of defective vascular development are already observed with the presence of highly unorganised endothelial cords rather than distinct paired dorsal aorta. By E10.5, both Sox7 complete knockout and FLK1-specific deletion of Sox7 lead to widespread vascular defects. In contrast, while SOX7 is expressed in the earliest specified blood progenitors, the VAV-specific deletion of Sox7 does not affect the hematopoietic system. Together, our data reveal the unique role of SOX7 in vasculogenesis and angiogenesis during embryonic development.
    Citation
    SOX7 expression is critically required in FLK1-expressing cells for vasculogenesis and angiogenesis during mouse embryonic development. 2017, 146: 31-41 Mech Dev
    Journal
    Mechanisms of Development
    URI
    http://hdl.handle.net/10541/620472
    DOI
    10.1016/j.mod.2017.05.004
    PubMed ID
    28577909
    Type
    Article
    Language
    en
    ISSN
    1872-6356
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.mod.2017.05.004
    Scopus Count
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    All Paterson Institute for Cancer Research

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